Currently, stent devices for preventing restenosis by supplying a cardiovascular or luminal support or reinforcement are widely used, but they have a significant clinical problem of restenosis with rates ranging 20˜40%. Mechanical intervention via stents have a low effect on the treatment of neointimal proliferation resulting from a complex immune response causing the enlargement and disruption of atherosclerotic plaques. This is because neointimal proliferation causes inflammation due to the initial enlargement and disruption of atherosclerotic lesions, so that a series of cellular events that activate an immune system are induced and cytokine that stimulates cell proliferation in the smooth muscle layer of the vessel media is released. This stimulation of cell proliferation can lead to coronary vessel restenosis.
In a recent attempt to cope with the problem of neointimal proliferation, drug-releasing stents coated with immune inhibitors or therapeutic agents are widely used. Immune inhibitors, such as rapamycin, prevent the initiation of DNA synthesis by targeting the G1-stage cells. Therapeutic agents, such as paclitaxel and other taxane derivatives, act on cells of the M-stage among stages known as the cell cycle, in the cellular DNA level, by preventing the dissolution of microtubules and interfering with cellular division. These strategies have significant advantages, but there are not only limitations in the duration of drug effect around the stents but also the risk of undesired systemic toxicity.
Accordingly, there is a need for an improved drug-coated stent which can mitigate the problem of early rapid release of drugs at the stent sites and improve the problem of limitations in therapeutic effects, which can be caused in the case of a single drug.